It has been found earlier in Lehninger's Laboratory [24] that oxidation of endogenous PN mitochondria induced by oxalacetic acid (OAA) brings about the release of accumulated Ca2+. Analysis of possible mechanism of this phenomenon has shown that OAA has protonophore activity on mitochondria and BPM unlike the malate--the product of enzymic reduction of OAA in the presence of NAD . H. OAA-induced permeability of BPM and mitochondria membranes for H+ is observed at pH 7.5-8.0 and is insignificant at pH 7.0 and lower. Possible function of OAA as a soft uncoupler-protonophore controlled by metabolism is discussed, in particular--in connection with Ca2+ transport in mitochondria.